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Faculty Detail    
Name MICHAL MRUG
 
Campus Address THT 611J Zip 0007
Phone  205-934-9509
E-mail  mmrug@uab.edu
Other websites Physician Profile
Publications (PubMed)
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Medicine  Med - Nephrology Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Professor
Center  Heflin Genetics Center  Heflin Genetics Center Professor
Center  General Clinical Research Center  Nephrology Research & Training Center Professor

Biographical Sketch 
Dr. Mrug received his M.D. at the Charles University in Prague, Czech Republic. He completed his internship and residency in Internal Medicine at the University of South Alabama in Mobile and fellowship in Nephrology at the University of Alabama at Birmingham (UAB). In 2004, he joined the UAB Division of Genetic and Translational Medicine as Instructor of Medicine and in 2005 was promoted to Assistant Professor. In 2008, he joined the UAB Division of Nephrology. Dr. Mrug is certified by the American Board of Internal Medicine by the Subspecialty Board on Nephrology. His clinical interests center on evaluation and management of adult patients with polycystic kidney disease (PKD). His current research focuses on the identification of specific genes and molecular pathway that modulate the severity of PKD and its progression.

Society Memberships
Organization Name Position Held Org Link
American Physiological Society    http://www.the-aps.org 
American Society of Nephrology    http://www.asn-online.org 



Research/Clinical Interest
Title
Pathogenesis of polycystic kidney disease progression
Description
Polycystic kidney disease (PKD) progression in both people and mouse models is highly variable. Specific biological processes that contribute to this variability remain largely unknown. Dr. Mrug’s current research focus is on the identification of biological processes and molecular pathways that modulate PKD progression. Their identification represents critical step for the discovery of new markers that would predict PKD course and for the development of novel therapies to cure PKD.

Selected Publications 
Publication PUBMEDID
Lever JM, Hull TD, Boddu R, Pepin ME, Black LM, Adedoyin OO, Yang Z, Traylor AM, Jiang Y, Li Z, Peabody JE, Eckenrode HE, Crossman DK, Crowley MR, Bolisetty S, Zimmerman KA, Wende AR, Mrug M, Yoder BK, Agarwal A, George JF. Resident macrophages reprogram toward a developmental state after acute kidney injury. JCI Insight. 2019 Jan 24;4(2). pii: 125503. doi: 10.1172/jci.insight.125503.  30674729 
Zimmerman KA, Gonzalez NM, Chumley P, Chacana T, Harrington LE, Yoder BK, Mrug M. Urinary T cells correlate with rate of renal function loss in autosomal dominant polycystic kidney disease. Physiol Rep. 2019 Jan;7(1):e13951. doi: 10.14814/phy2.13951.  30632307 
Zimmerman KA, Bentley MR, Lever JM, Li Z, Crossman DK, Song CJ, Liu S, Crowley MR George JF, Mrug M, Yoder BK. Single-cell RNAseq identifies candidate renal resident macrophage gene expression signatures across species. J Am Soc Nephrol. 2019  30948627 
Shan D, Rezonzew G, Mullen S, Roye R, Zhou J, Chumley P, Revell DZ, Challa A, Kim H, Lockhart ME, Schoeb TR, Croyle MJ, Kesterson RA, Yoder BK, Guay-Woodford LM, Mrug M. Heterozygous Pkhd1C642* mice develop cystic liver disease and proximal tubule ectasia that mimics radiographic signs of medullary sponge kidney. Am J Physiol Renal Physiol. 2019 Mar 1;316(3):F463-F472. doi: 10.1152/ajprenal.00181.2018.  30600684 
McKenzie KA, El Ters M, Torres VE, Harris PC, Chapman AB, Mrug M, Rahbari-Oskoui FF, Bae KT, Landsittel DP, Bennett WM, Yu ASL, Mahnken JD. Relationship between caffeine intake and autosomal dominant polycystic kidney disease progression: a retrospective analysis using the CRISP cohort. BMC Nephrol. 2018 Dec 27;19(1):378. doi: 10.1186/s12882-018-1182-0.  30591038 
Chumley P, Zhou J, Mrug S, Chacko B, Parant JM, Challa AK, Wilson LS, Berryhill TF, Barnes S, Kesterson RA, Bell PD, Darley-Usmar VM, Yoder BK, Mrug M. Truncating PKHD1 and PKD2 mutations alter energy metabolism. Am J Physiol Renal Physiol. 2019 Mar 1;316(3):F414-F425. doi: 10.1152/ajprenal.00167.2018.  30566001 
Chebib FT, Perrone RD, Chapman AB, Dahl NK, Harris PC, Mrug M, Mustafa RA, Rastogi A, Watnick T, Yu ASL, Torres VE. A Practical Guide for Treatment of Rapidly Progressive ADPKD with Tolvaptan. J Am Soc Nephrol. 2018 Oct;29(10):2458-2470. doi: 10.1681/ASN.2018060590.   30228150 
Lewis WR, Bales KL, Revell DZ, Croyle MJ, Engle SE, Song CJ, Malarkey EB, Uytingco CR, Shan D, Antonellis PJ, Nagy TR, Kesterson RA, Mrug MM, Martens JR, Berbari NF, Gross AK, Yoder BK. Mks6 mutations reveal tissue- and cell type-specific roles for the cilia transition zone. FASEB J. 2019 Jan;33(1):1440-1455. doi: 10.1096/fj.201801149R.   30133325 
Billot K, Coquil C, Villiers B, Josselin-Foll B, Desban N, Delehouzé C, Oumata N, Le Meur Y, Boletta A, Weimbs T, Grosch M, Witzgall R, Saunier S, Fischer E, Pontoglio M, Fautrel A, Mrug M, Wallace D, Tran PV, Trudel M, Bukanov N, Ibraghimov-Beskrovnaya O, Meijer L. Casein kinase 1-epsilon and 1-alpha as novel players in polycystic kidney disease and mechanistic targets for (R)-roscovitine and (S)-CR8. Am J Physiol Renal Physiol. 2018 Jul 1;315(1):F57-F73.  29537311 
Yu ASL, Shen C, Landsittel DP, Harris PC, Torres VE, Mrug M, Bae KT, Grantham JJ, Rahbari-Oskoui FF, Flessner MF, Bennett WM, Chapman AB; Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP). Baseline total kidney volume and the rate of kidney growth are associated with chronic kidney disease progression in Autosomal Dominant Polycystic Kidney Disease. Kidney Int. 2018 Mar;93(3):691-699.   29290310 
Yu ASL, Shen C, Landsittel DP, Grantham JJ, Cook LT, Torres VE, Chapman AB, Bae KT, Mrug M, Harris PC, Rahbari-Oskoui FF, Shi T, Bennett WM; Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP). Long-term trajectory of kidney function in autosomal-dominant polycystic kidney disease. Kidney Int. 2019 Mar 4. pii: S0085-2538(19)30104-8. doi  30922668 

Keywords
polycystic kidney disease, innate immunity, genome-wide expression profiling, animal models